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Journal of Neuroscience, Vol 15, 5765-5778, Copyright © 1995 by Society for Neuroscience
BDNF enhances the differentiation but not the survival of CNS stem cell- derived neuronal precursors
S Ahmed, BA Reynolds and S Weiss
Department of Anatomy, University of Calgary Faculty of Medicine, Alberta, Canada.
We have previously reported the isolation of an EGF-responsive precursor
from the embryonic and adult mouse striatum. This precursor exhibits self
renewal and the ability to produce a sphere of undifferentiated cells which
can be induced to differentiate into neurons and glia. RT-PCR analysis of
these spheres of undifferentiated cells revealed the expression of mRNA for
the trkB neurotrophin receptor, both with and without the catalytic domain,
and little or no expression of trkA or trkC. We examined the actions of
BDNF on the fate of EGF-generated neural precursors. Ten days after a
one-time exposure to BDNF, single EGF-generated spheres showed a twofold
increase in neuron number and a marked enhancement in neurite outgrowth.
Examination of neuronal nuclei with immunochemical probes for c-fos and
bromodeoxyuridine revealed that the actions of BDNF were directly upon
neuronal cells and did not involve division of neuronal precursors. The
twofold increase in neuronal number due to BDNF, observed after 10 d in
vitro, was significantly reduced after 21 d in vitro and was not apparent
at 27 d in vitro. Quantitative analyses revealed that while repeated
application of BDNF did not prevent the loss of neuron number over time, it
did result in a significant increase in neurite numbers. Moreover, delayed
addition of BDNF mimicked the increase in neuronal numbers seen when BDNF
was present throughout. These BDNF actions did not appear to involve the
enhancement of a novel neuronal phenotype, with all effects being due to
increase in the numbers and neurite outgrowth of neurons that colocalize
GABA and substance P. These findings suggest that BDNF markedly enhances
the antigenic and morphologic differentiation of EGF-generated neuronal
precursors. BDNF alone does not appear to act as a survival factor for
neuronal precursors nor is it sufficient for preventing their death over
time.
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